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Cellular senescence plays a central role in organismal aging as demonstrated by the extension of healthy lifespan after selective removal of senescent cells. Indeed, agents that kill senescent cells (senolytics), are near to entering human clinical trials. Senescent cells show increased size, flat morphology and increased adhesion to the extracellular matrix with large focal adhesions. This transition is associated with decreased levels of the focal adhesion adapter and Rac/Cdc42 GEF ?PIX. Reducing levels of ?PIX induced cellular senescence and organismal aging in both invertebrate and vertebrate systems. Human genetic evidence also indicates a role for integrin signaling in aging. ?PIX knockdown induces cellular senescence through abnormal ?1 integrin trafficking, signaling and ROS generation. These data provide a mechanistic link that supports the long-known correlation between integrin-mediated adhesion and cellular senescence. Integrins and associated proteins are thus promising targets for anti-aging therapy.

Speaker

Eung-Gook Kim

Organisation: Department of Biochemistry, Chungbuk National University College of Medicine, Cheongju, Korea